Brauer R W, Dutcher J A
J Appl Physiol (1985). 1987 Apr;62(4):1635-46. doi: 10.1152/jappl.1987.62.4.1635.
Inert gas narcotics increase intrinsic pressure tolerance (1,000Pc) in CD-1 mice but interfere with development of the protective responses raising seizure thresholds during slower compression (e.g., 60Pc). This secondary narcotic effect can block up to 40% of the total attainable increase in Pc. The narcosis susceptible moiety of this compression rate effect develops early, whereas a narcosis resistant remnant accounts for increase in Pc occurring after 90 min of compression or pressure exposure. Pressure conditioning by multiday pressure exposure entails increases in both 60Pc and 1,000Pc and in virtual annullment of the compression rate effect. The effect can be completely blocked by narcotic gases in the conditioning atmosphere. In addition to blocking part of the compression rate effect the presence of narcotic gases under these conditions can reverse the effects of previously established pressure conditioning. 60Pc regresses much more slowly under these conditions than 1,000Pc. Either reversal rate is much more rapid in air at 1 ATA than at 80 ATA under 0.9 atm N2O. The implications of these data are discussed with regard to evaluation of the hypothesis of antagonism between inert gas narcotics and high pressures and to elaboration of the monoamine hypothesis to account for the modification of the compression rate effect by narcotic gases.
惰性气体麻醉剂可提高CD-1小鼠的固有压力耐受性(1000Pc),但在较慢压缩过程中(例如60Pc)会干扰提高癫痫阈值的保护性反应的发展。这种继发性麻醉作用可阻断高达40%的Pc总增加值。这种压缩速率效应的麻醉易感部分发展较早,而麻醉抗性残余部分则是压缩或压力暴露90分钟后Pc增加的原因。通过多日压力暴露进行压力预处理会使60Pc和1000Pc均增加,并几乎消除压缩速率效应。预处理环境中的麻醉气体可完全阻断这种效应。在这些条件下,麻醉气体的存在除了会阻断部分压缩速率效应外,还会逆转先前建立的压力预处理的效果。在这些条件下,60Pc的恢复比1000Pc慢得多。在1ATA的空气中,任何一种逆转速率都比在0.9个大气压的N2O下80ATA时快得多。讨论了这些数据对于评估惰性气体麻醉剂与高压之间拮抗作用假说以及阐述单胺假说以解释麻醉气体对压缩速率效应的影响的意义。